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Blood, 1 August 2006, Vol. 108, No. 3, pp. 947-955.
Prepublished online as a Blood First Edition Paper on April 13, 2006; DOI 10.1182/blood-2005-12-4812.
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Submitted December 6, 2005
Accepted February 27, 2006
The apoptotic cell receptor CR3, but not v 5, is a regulator of human dendritic cell immunostimulatory function
Mojca Skoberne, Selin Somersan, Wanda Almodovar, Tuan Truong, Kseniya Petrova, Peter M Henson, and Nina Bhardwaj*
NYU School of Medicine, New York, NY, USA
Program in Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO, USA
* Corresponding author; email: bhardn02{at}med.nyu.edu.
Dendritic cells (DCs) that capture apoptotic cells (AC) in the steady-state mediate peripheral tolerance to self-antigens. ACs are recognized by an array of receptors on DCs, the redundancy of which is not completely defined. We made use of an AC surrogate system to address the individual roles of the v 5 and complement receptors (CR) in the phagocytosis and induction of immunity. CR3 and CR4, while substantially less efficient than v 5 in internalizing ACs, initiate signals that render DCs tolerogenic. Responding T cells show impaired proliferation and IFN production, and subsequently die by apoptosis. While tolerogenic DCs are not induced via v 5, co-ligation of CR3 and v 5 maintains the DCs[[rad]] tolerogenic profile. This immunomodulatory role, however, is countered by a significant inflammatory stimulus such as bacterial infection. Overall, our data suggest that under steady state conditions, signaling via CRs predominates to render DCs tolerogenic.

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